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ENDOCRINE > PRIMARY HYPERALDOSTERONISM > Flashcards

PRIMARY HYPERALDOSTERONISM Flashcards

1
Q

What is the function of the adrenal cortex?

three

A
  1. steroid hormone function biosynthesis and regulation
  2. diagnostic testing
  3. adrenocortical insufficiency states (acute and chronic adrenal insufficiency)
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2
Q

What are the 2 adrenocortical excess states?

A
  1. cushing’s syndrome
  2. conn syndrome
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3
Q

Adrenal medulla:

what does it do and what can occur at that level?

A

catecholamine synthesis, metabolism, receptors and functions

pheochromocytoma/paragangliomas occur here

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4
Q

What is the definitive zone of the fetal adrenal gland?

A

the principal site of glucocorticoid and mineralcorticoid synthesis

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5
Q

What is the fetal zone of the fetal adrenal gland?

A

androgenic precursors, which the placenta converts to various types of estrogens

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6
Q

what are the cortexes of the mature adrenal gland?

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
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7
Q

Where is the medulla?

A

at the very bottom of both fetal and mature adrenal gland gradient

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8
Q

What is the function of the zona glomerulosa?

two things

A
  1. MINERALCORTICOIDS
  2. sodium resorption in the kidney, thus electrolyte balance, intravascular volume, and blood pressure
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9
Q

What is the function of the zona fasciculata?

A
  1. GLUCOCORTICOIDS
  2. named for their carbohydrate-mobilizing activity
  3. ubiquitous physiologic regulators, influencing a wide variety of bodily functions
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10
Q

What is the function of the zona reticularis?

A
  1. SEX STEROIDS
  2. no known physiologic role
  3. secondary characteristics in women, overproduction can result in virilization
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11
Q

Biosynthesis of Aldosterone:

A

pregnenolone-> progesterone-> 11- deoxycorticosterone-> corticosterone-> aldosterone

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12
Q

biosynthesis of cortisol:

A

17-hydroxyoregnenolone-> 17-hydroxyprogesterone-> 11-deoxycortisol-> cortisol

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13
Q

biosynthesis of androstenedione:

A

Dehydroepiandrosterone (DHEA)-> Androsteneidone

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14
Q

How is aldosterone regulated?

A

renin-angiotensin system

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15
Q

what is primary hyperaldosteronism also known as?

A

conn syndrome

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16
Q

significance of primary hyperaldosteronism?

four things

A
  1. inappropriately high aldosterone production, autonomous of major regulators of secretion (angi II, potassium)
  2. causes HTN, CV damage, Na retention, suppression of plasma renin, increased K excretion (hypokalemia 9-37%)
  3. increasingly recognized, >5% and possibly >10% of hypertensive patients
  4. higher CV morbidity and mortality than age and sex matched patients with essential HTN and same degree BP elevation
17
Q

Who should be screened ?

A
  1. sustained BP >150/100 on each of 3 measurements on different days
  2. HTN (BP >140/90) resistant to 3 conventional antihypertensive drugs (including a diuretic)
  3. controlled BP (<140/90) on 4+ antihypertensive agents
  4. HTN plus spontaneous or diuretic-induced hypokalemia, adrenal incidentaloma, sleep apnea, FMHx of early onset HTN or cerebrovascular accident at young age (<40 years), first degree relatives of pt w/ primary hyperaldosteronism (PA)
18
Q

Patho of hyperaldosteronism:

A
  1. MOST COMMON: ADRENAL ADENOMA
  2. uni or bilat adrenal hyperplasia
  3. adrenal carcinoma
  4. inherited conditions of familial hyperaldosteronism -> familial hyperaldosteroniam T1 (FH-I),aka glucocorticoid remediable aldosteronism —> recombination between 11betahydroxylase (CYP11B1) and aldosterone synthase (CYP11B2), expression of mutant form of CYP 11B2 drives transcription under control of ACTH
  5. there also exists FH-II and FH-III
19
Q

screening: what is the screening for hyperaldosteronism?

A
  1. PLASMA ALDOSTERONE/RENIN RATIO (ARR)
    - collect samples in morning after patients out of bed for at least 2 hours, usually after they have been seated for 5-15 min
    - unrestricted dietary salt intake, ideally K+- replete
    - mineralcorticoid receptor anatagonists withdrawn for atleast 4 weeks
    - complete cessation of all interfering antihypertensives is usually not necessary
20
Q

increased renin and decreased aldosterone indicates what?

A

a kidney problem

21
Q

decreased renin and increased aldosterone indicates what?

A

conn syndrome

22
Q

increased renin and normal aldosterone indicates what?

A

salt sensitivity (AA)

23
Q

What are the confirmatory tests for hyperaldosteronism?

A
  1. oral Na loading test -checking sodium sensitivity
  2. saline infusion test (seated better sensitivity than recumbent)
  3. furosemide upright test -checks pressure
  4. captopril challenge test - inhibits ace. if still high after test, confirmatory
24
Q

what is the choice of test based on?

A

pt safety, cost, pt compliance, local experience/expertise

25
Q

when is confirmatory testing not needed?

A

spontaneous hypokalemia, plasma renin below detection level + plasma aldosterone concentration >20 ng/dL

26
Q

What test do you start with in diagnosing hyperaldosteronism and why?

A
  1. CT. This is to exclude large masses that may represent adrenocortical carcinoma, can also help interventional radiology before adrenal venous sampling (AVS)
27
Q

What is pre-op treatment?

A

HTN and hypokalmeia should be well controlled

28
Q

What is post-op treatment?

A
  1. measure plasma aldosterone and renin activity shortly after surgery
  2. Day 1: d/c K supplementation and Spiro, and reduce antihypertensive therapy if u can
  3. generous sodium diet to avoid hyperkalemia that can develop from hyperaldosteronism d/t chronic contralat. adrenal glands suppression
  4. BP normalizes or shows improvement in 1-6 months, but can continue to fall for up to 1 year.
29
Q

Hyperaldosteronism medical management:

A

-MINERALCORTICOID RECEPTOR ANTAGONISTS-
1. Spironolactone 1st gen ; reduces SBP 25%, DBP 22%; half of patients can manage w/ spiro monotherapy; non-selective and has anti-androgen and progesterone agonist effects
2. Eplerenone 2nd gen- shorter half life and lower MR affinity compared to spiro; 25 mg; new and more expensive; selective MR antagonist
3. 3rd gen MR antagonists and aldosterone synthase inhibitors are new to market/in development

30
Q

look at physio slide

A

…

31
Q

medical management of FH-1/GRA

A
  1. glucocorticoid to partially suppress pituitary ACTH secretion
    • dosage varies in kids by age and body weight; taken at bedtime to suppress early morn ACTH surge; use lowest possible dose to normalize BP and/or serum K; avoid over-treatment/iatrogenic Cushing syndrome
  2. long acting glucocorticoids preferred
    • dexa and prednisone
32
Q

what are the 2 things found in the mature adrenal gland?

A
  1. cortex
  2. medulla

ENDOCRINE (18 decks)

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